Abnormalities in social behavior and cognition are among the many profound consequences of prenatal exposure to alcohol. Such deficits may underlie or exacerbate deficits in other important areas such as school performance, and contribute to the prevalence of clinical behavioral problems such as conduct disorder. At present there are no long-term treatments for abnormal social behavior in children with Fetal Alcohol Spectrum Disorder (FASD). Despite the importance of these problems, surprisingly little is known about the neurobiological, behavioral, and environmental bases of alcohol-related deficits in social behavior and cognition. However, such information is critical for developing and evaluating therapeutic approaches. The objective of the proposed research is to better understand the neurobiological bases of alcohol-related impairments in social behavior. Due to the broad range of factors that could contribute to alcohol-related deficits in social behavior in FASD children, meeting this objective will require systematic research using animal models of prenatal alcohol exposure. Damage to the OPFC has been linked to abnormal social behavior in many species, providing the rationale for the proposed experiments. The specific aims of the proposed research focus on identifying the effects of moderate prenatal ethanol exposure on socially induced structural plasticity in OPFC neurons and immediate early gene expression in OPFC neurons as a marker of neural activity during social interaction. The proposed research will assess whether prenatal alcohol exposure is associated with a decreased capacity for experience-dependent changes in the dendritif fields of individual neurons as a result of social experience and whether such a diminished capacity is related to a decrease in the responsiveness of OPFC neurons to social stimuli and interaction. Once identified, future research can be undertaken to pursue relevant treatments and identify factors that contribute to or alleviate alcohol-induced behavioral impairments. Importantly, identification of impairments in structural plasticity or neural activation in the rat OPFC may lead to therapeutic approaches in humans, and help bridge the gap between basic and clinical research to advance our knowledge regarding the consequences of prenatal alcohol exposure. [unreadable] [unreadable] [unreadable]